Conscious guinea-pigs received platelet activating factor (PAF, 0.03-0.25 μg/kg, i.v.) and colloidal carbon (C, tracer for microvascular leakage). Fifteen min later the animal was killed and C-labelled microvessels (leakage) were detected in the mucosal/submucosal region of tracheal and bronchial sections. PAF was more potent than LTD4 or histamine. The numbers of leaky vessel were dose-related, arterioles and arteries were not affected, leaky vessels were seen from proximal trachea to intrapulmonary bronchi and carbon was not apparent in the alveolar wall. The effect was quick in onset, of short duration, could be repeated, was not produced by lyso-PAF and was unaffected by thrombocytopaenia (produced by an antiserum). Thrombocytopaenia itself did not cause leaky vessels in the airways nor affect histamine responses. Thus, PAF causes an increase in microvascular leakage in the conducting airways, which is not dependent on platelets. The affected vessels are probably postcapillary bronchial venules and PAF may act via an endothelial cell receptor in these microvessels. This leakage effect of PAF in the airways could contribute to features of bronchial asthma.